Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis

IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions...

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Veröffentlicht in:BBA clinical 2016-06, Vol.5, p.79-84
Hauptverfasser: Moresco, Rafael N., Speeckaert, Marijn M., Zmonarski, Slawomir C., Krajewska, Magdalena, Komuda-Leszek, Ewa, Perkowska-Ptasinska, Agnieszka, Gesualdo, Loreto, Rocchetti, Maria T., Delanghe, Sigurd E., Vanholder, Raymond, Van Biesen, Wim, Delanghe, Joris R.
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container_issue
container_start_page 79
container_title BBA clinical
container_volume 5
creator Moresco, Rafael N.
Speeckaert, Marijn M.
Zmonarski, Slawomir C.
Krajewska, Magdalena
Komuda-Leszek, Ewa
Perkowska-Ptasinska, Agnieszka
Gesualdo, Loreto
Rocchetti, Maria T.
Delanghe, Sigurd E.
Vanholder, Raymond
Van Biesen, Wim
Delanghe, Joris R.
description IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions. Therefore, urinary CD89 and TG2 could be potential biomarkers to identify active IgAN/HSPN. In this multicenter study, 160 patients with IgAN or HSPN were enrolled. Urinary concentrations of CD89 and TG2, as well as some other biochemical parameters, were measured. Urinary CD89 and TG2 were lower in patients with active IgAN/HSPN compared to IgAN/HSPN patients in complete remission (P
doi_str_mv 10.1016/j.bbacli.2016.02.002
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The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions. Therefore, urinary CD89 and TG2 could be potential biomarkers to identify active IgAN/HSPN. In this multicenter study, 160 patients with IgAN or HSPN were enrolled. Urinary concentrations of CD89 and TG2, as well as some other biochemical parameters, were measured. Urinary CD89 and TG2 were lower in patients with active IgAN/HSPN compared to IgAN/HSPN patients in complete remission (P<0.001). The CD89xTG2 formula had a high ability to discriminate active from inactive IgAN/HSPN in both situations: CD89xTG2/proteinuria ratio (AUC: 0.84, P<0.001, sensitivity: 76%, specificity: 74%) and CD89xTG2/urinary creatinine ratio (AUC: 0.82, P<0.001, sensitivity: 75%, specificity: 74%). Significant correlations between urinary CD89 and TG2 (r=0.711, P<0.001), proteinuria and urinary CD89 (r=−0.585, P<0.001), and proteinuria and urinary TG2 (r=−0.620, P<0.001) were observed. Determination of CD89 and TG2 in urine samples can be useful to identify patients with active IgAN/HSPN. •IgAN and HSPN are glomerular diseases with a common central pathogenic mechanism.•Anatomopathological analysis of renal biopsies is required for diagnosis.•Urinary CD89 and urinary TG2 are decreased in patients with active IgAN/HSPN.•The CD89xTG2 product has a high ability to discriminate active IgAN/HSPN.]]></description><identifier>ISSN: 2214-6474</identifier><identifier>EISSN: 2214-6474</identifier><identifier>DOI: 10.1016/j.bbacli.2016.02.002</identifier><identifier>PMID: 27051593</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Henoch-Schönlein purpura nephritis ; IgA nephropathy ; Myeloid IgA Fc alpha receptor ; Regular ; Transglutaminase-2</subject><ispartof>BBA clinical, 2016-06, Vol.5, p.79-84</ispartof><rights>2016 The Authors</rights><rights>2016 The Authors 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-b7cb80a8cdd3d7f0cb3d24b0ee5bf665eed2b8cbb59a6ff0d1d2156fb618888a3</citedby><cites>FETCH-LOGICAL-c463t-b7cb80a8cdd3d7f0cb3d24b0ee5bf665eed2b8cbb59a6ff0d1d2156fb618888a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802400/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802400/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27051593$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moresco, Rafael N.</creatorcontrib><creatorcontrib>Speeckaert, Marijn M.</creatorcontrib><creatorcontrib>Zmonarski, Slawomir C.</creatorcontrib><creatorcontrib>Krajewska, Magdalena</creatorcontrib><creatorcontrib>Komuda-Leszek, Ewa</creatorcontrib><creatorcontrib>Perkowska-Ptasinska, Agnieszka</creatorcontrib><creatorcontrib>Gesualdo, Loreto</creatorcontrib><creatorcontrib>Rocchetti, Maria T.</creatorcontrib><creatorcontrib>Delanghe, Sigurd E.</creatorcontrib><creatorcontrib>Vanholder, Raymond</creatorcontrib><creatorcontrib>Van Biesen, Wim</creatorcontrib><creatorcontrib>Delanghe, Joris R.</creatorcontrib><title>Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis</title><title>BBA clinical</title><addtitle>BBA Clin</addtitle><description><![CDATA[IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions. Therefore, urinary CD89 and TG2 could be potential biomarkers to identify active IgAN/HSPN. In this multicenter study, 160 patients with IgAN or HSPN were enrolled. Urinary concentrations of CD89 and TG2, as well as some other biochemical parameters, were measured. Urinary CD89 and TG2 were lower in patients with active IgAN/HSPN compared to IgAN/HSPN patients in complete remission (P<0.001). The CD89xTG2 formula had a high ability to discriminate active from inactive IgAN/HSPN in both situations: CD89xTG2/proteinuria ratio (AUC: 0.84, P<0.001, sensitivity: 76%, specificity: 74%) and CD89xTG2/urinary creatinine ratio (AUC: 0.82, P<0.001, sensitivity: 75%, specificity: 74%). Significant correlations between urinary CD89 and TG2 (r=0.711, P<0.001), proteinuria and urinary CD89 (r=−0.585, P<0.001), and proteinuria and urinary TG2 (r=−0.620, P<0.001) were observed. Determination of CD89 and TG2 in urine samples can be useful to identify patients with active IgAN/HSPN. •IgAN and HSPN are glomerular diseases with a common central pathogenic mechanism.•Anatomopathological analysis of renal biopsies is required for diagnosis.•Urinary CD89 and urinary TG2 are decreased in patients with active IgAN/HSPN.•The CD89xTG2 product has a high ability to discriminate active IgAN/HSPN.]]></description><subject>Henoch-Schönlein purpura nephritis</subject><subject>IgA nephropathy</subject><subject>Myeloid IgA Fc alpha receptor</subject><subject>Regular</subject><subject>Transglutaminase-2</subject><issn>2214-6474</issn><issn>2214-6474</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp9kd1uFSEUhYmxsU3tGxjDZb2YEZj_G5PmaGuTJl60vSb87DnDcQZGYI45b-KT-AK-WGlPrfWmhAQIe63N4kPoHSU5JbT-uMmlFGo0OUunnLCcEPYKHTFGy6wum_L1s_0hOglhQwihrGq6hr5Bh6whFa264gj9uvXGCr_D0w5GZzS-XJ_hc4XFOA8Ce1AwR-fx6epz233AwmocvbBhPS5RTEkZIGNYBGzhJ5bGTcJ_Bx9wnzRCRbOFB0ML8-DdLOKwe_AYwDo1ZNdq-PPbjmAsnhefpthXmmjCW3TQizHAyeN6jG7Pv9ysvmZX3y4uV2dXmSrrImayUbIlolVaF7rpiZKFZqUkAJXs67oC0Ey2SsqqE3XfE001o1Xdy5q2aYjiGH3a-86LnEArsCngyGdvUpYdd8Lw_2-sGfjabXnZElYSkgxOHw28-7FAiHwyQcE4CgtuCZw2Tdc2XdmxVFruS5V3IXjon9pQwu-58g3fc-X3XDlhPHFNsvfPn_gk-kvxXwZIH7U14HlQBqwCbRLByLUzL3e4A-jOum8</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Moresco, Rafael N.</creator><creator>Speeckaert, Marijn M.</creator><creator>Zmonarski, Slawomir C.</creator><creator>Krajewska, Magdalena</creator><creator>Komuda-Leszek, Ewa</creator><creator>Perkowska-Ptasinska, Agnieszka</creator><creator>Gesualdo, Loreto</creator><creator>Rocchetti, Maria T.</creator><creator>Delanghe, Sigurd E.</creator><creator>Vanholder, Raymond</creator><creator>Van Biesen, Wim</creator><creator>Delanghe, Joris R.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160601</creationdate><title>Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis</title><author>Moresco, Rafael N. ; Speeckaert, Marijn M. ; Zmonarski, Slawomir C. ; Krajewska, Magdalena ; Komuda-Leszek, Ewa ; Perkowska-Ptasinska, Agnieszka ; Gesualdo, Loreto ; Rocchetti, Maria T. ; Delanghe, Sigurd E. ; Vanholder, Raymond ; Van Biesen, Wim ; Delanghe, Joris R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-b7cb80a8cdd3d7f0cb3d24b0ee5bf665eed2b8cbb59a6ff0d1d2156fb618888a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Henoch-Schönlein purpura nephritis</topic><topic>IgA nephropathy</topic><topic>Myeloid IgA Fc alpha receptor</topic><topic>Regular</topic><topic>Transglutaminase-2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moresco, Rafael N.</creatorcontrib><creatorcontrib>Speeckaert, Marijn M.</creatorcontrib><creatorcontrib>Zmonarski, Slawomir C.</creatorcontrib><creatorcontrib>Krajewska, Magdalena</creatorcontrib><creatorcontrib>Komuda-Leszek, Ewa</creatorcontrib><creatorcontrib>Perkowska-Ptasinska, Agnieszka</creatorcontrib><creatorcontrib>Gesualdo, Loreto</creatorcontrib><creatorcontrib>Rocchetti, Maria T.</creatorcontrib><creatorcontrib>Delanghe, Sigurd E.</creatorcontrib><creatorcontrib>Vanholder, Raymond</creatorcontrib><creatorcontrib>Van Biesen, Wim</creatorcontrib><creatorcontrib>Delanghe, Joris R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BBA clinical</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moresco, Rafael N.</au><au>Speeckaert, Marijn M.</au><au>Zmonarski, Slawomir C.</au><au>Krajewska, Magdalena</au><au>Komuda-Leszek, Ewa</au><au>Perkowska-Ptasinska, Agnieszka</au><au>Gesualdo, Loreto</au><au>Rocchetti, Maria T.</au><au>Delanghe, Sigurd E.</au><au>Vanholder, Raymond</au><au>Van Biesen, Wim</au><au>Delanghe, Joris R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis</atitle><jtitle>BBA clinical</jtitle><addtitle>BBA Clin</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>5</volume><spage>79</spage><epage>84</epage><pages>79-84</pages><issn>2214-6474</issn><eissn>2214-6474</eissn><abstract><![CDATA[IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions. Therefore, urinary CD89 and TG2 could be potential biomarkers to identify active IgAN/HSPN. In this multicenter study, 160 patients with IgAN or HSPN were enrolled. Urinary concentrations of CD89 and TG2, as well as some other biochemical parameters, were measured. Urinary CD89 and TG2 were lower in patients with active IgAN/HSPN compared to IgAN/HSPN patients in complete remission (P<0.001). The CD89xTG2 formula had a high ability to discriminate active from inactive IgAN/HSPN in both situations: CD89xTG2/proteinuria ratio (AUC: 0.84, P<0.001, sensitivity: 76%, specificity: 74%) and CD89xTG2/urinary creatinine ratio (AUC: 0.82, P<0.001, sensitivity: 75%, specificity: 74%). Significant correlations between urinary CD89 and TG2 (r=0.711, P<0.001), proteinuria and urinary CD89 (r=−0.585, P<0.001), and proteinuria and urinary TG2 (r=−0.620, P<0.001) were observed. Determination of CD89 and TG2 in urine samples can be useful to identify patients with active IgAN/HSPN. •IgAN and HSPN are glomerular diseases with a common central pathogenic mechanism.•Anatomopathological analysis of renal biopsies is required for diagnosis.•Urinary CD89 and urinary TG2 are decreased in patients with active IgAN/HSPN.•The CD89xTG2 product has a high ability to discriminate active IgAN/HSPN.]]></abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>27051593</pmid><doi>10.1016/j.bbacli.2016.02.002</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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source Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access
subjects Henoch-Schönlein purpura nephritis
IgA nephropathy
Myeloid IgA Fc alpha receptor
Regular
Transglutaminase-2
title Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis
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